The American Roots of Social Epidemiology and its Transnational Circulation. From the African-American Hypertension Enigma to the WHO's ...
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Gesnerus 77/1 (2020) 35–63, DOI: 10.24894/Gesn-en.2020.77002
The American Roots of Social Epidemiology and its
Transnational Circulation. From the African-American
Hypertension Enigma to the WHO’s Recommendations
Mathieu Arminjon
Abstract
In 2008, the Commission on Social Determinants of Health at the World
Health Organisation published a report demonstrating the existence of a so-
cio-economic gradient for health. Though health inequalities had been ap-
parent since at least the 19th century, the report introduced a bio-psycho-so-
cial aetiological model that was absent from 19th century social medicine, as
well as from former WHO documents. To bio-psycho-social epidemiologists
stress associated with social status is the main cause of morbidity and death.
Here I begin by noting that the history social epidemiologists have writ-
ten for their field tends to inscribe their work in continuity with 19th century
social medicine. This contributes towards minimizing the epistemological
and contextual transformations that led bio-psycho-social epidemiology to
initiate a profound transformation in international health policy. Adopting
an epistemological and transnational perspective, I firstly argue that bio-psy-
cho-social epidemiology emerged from René Dubos’ historical and episte-
mological critique of the foundation of 19th century social medicine. I sec-
ondly show how the political and epistemological research program
elaborated by Dubos developed in the US context, which was characterized
both by a growing concern for chronic diseases and for racial inequalities.
Finally, I show that through its transnational circulation in the United
Kingdom, bio-psycho-social epidemiology was “de-racialized”. This step
was a prerequisite for its aetiological model to be integrated into interna-
tional public health strategies and to transform them.
Keywords: biopsychosocial, stress, emotions, social epidemiology, René
Dubos, Thomas McKeown, WHO
Mathieu Arminjon, School of Health Sciences (HESAV), University of Applied Sciences and
Arts Western Switzerland (HES-SO), Avenue de Beaumont 21, CH-1011 Lausanne,
mathieu.arminjon@hesav.ch
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via free accessMaking the History of Social Epidemiology
In 1998, two British social epidemiologists, Richard Wilkinson and Michael
Marmot, published a report1 on the social determinants of health for the Re-
gional Office for Europe at the World Health Organisation (WHO). In 2005,
Marmot was appointed Chair of the Commission on Social Determinants of
Health for the WHO. In 2008, the commission published a new report2 con-
taining recommendations for closing the gap of social inequalities of health
in one generation. Two points arise from these reports: (1) the existence of a
socio-economic gradient, that Marmot had summarised elsewhere as “the
higher the social position, the better the health”, 3 which is essentially (2) the
result of bio-psycho-social stress induced by social inequalities.
Social determinants of health have been central to the WHO’s policies
since 1948,4 yet, the reports confi rm that a significant epistemological step
has been taken: By ratifying the report, the WHO recognised bio-psy-
cho-social epidemiology’s most radical thesis: stress associated with social
status, is the main cause of morbidity and mortality. In other words, bio-psy-
cho-social epidemiologists managed to completely overturn theories of pub-
lic health that generally focused on an individual’s lifestyle, in favour of the
idea that changing social conditions, as well as the way capital is distributed,
would make people healthier.
Paradoxically, social epidemiologists minimize the intellectual transfor-
mations brought about by bio-psycho-social epidemiology. To Nancy Krieger,
Marmot only rediscovered, “with some fanfare”, 5 the socio-economic gradi-
ent, originally discovered by Louis René Villermé (1782–1863). For some
others, social epidemiologists are only “rediscovering the role of the physical
and social environment”,6 or “rediscover the powerful effect of social condi-
tions in shaping morbidity and mortality.”7 If so, one would infer from this
“rhetoric of rediscovery” that bio-psycho-social epidemiology is nothing
more than a rediscovery of the work and findings of three central figures of
19th century social medicine: Villermé, Rudolf Virchow (1821–1902), and Ed-
win Chadwick (1800–1890).
Here I argue that these quotations understate aspects of the history of so-
cial epidemiology, especially the extent to which the bio-psycho-social
1 Wilkinson/Marmot 1998.
2 CSDH 2008.
3 Marmot 2006, 1304.
4 Irwin/Scali 2007.
5 Krieger 2011, 78.
6 McIntyre/Ellaway 2000, 332.
7 Susser/Myer 2007, 208.
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via free accessmodel emerged as an explicit attempt to operate a rupture with 19th century
social medicine. At present, neither the history of public health, nor the his-
tory of social epidemiology offer extensive genealogy8 able to replace in
their context the transformations that paved the way for the development of
social epidemiology. This paper intends to help fill that void by retracing the
intellectual trajectories that led actors to conceptualize the epistemological
foundations of the field.
Given that Marmot and Wilkinson are British, one could expect to fi nd
some elements of the history of bio-psycho-social epidemiology’s origin in
the history of British public health. Through the National Health Service
(NHS), British public health culture is historically characterised by what
Marmot calls an “obsession with class”.9 Moreover, in the 1940s–1950s, the
“new public health”10 embodied by a generation of British epidemiologists –
John Ryle (1889–1950), Thomas McKeown (1912–1988), Jerry Morris (1910–
2009), Geoffrey Rose (1926–1993) – showed a real interest in the social de-
terminants of disease. Dorothy Porter, though, has demonstrated that this
interest faded in the early 1960s.11
Why insist here on exploring the origin of bio-psycho-social epidemiol-
ogy from a national perspective? The purpose of this article is to show that
the transformation of the WHO’s understanding of social inequality is the
culmination of a chain of transformations that started in the 1940s–1950s,
when a new generation of actors, active in the field of public health, recon-
sidered, from a historical point of view, the epistemological foundations and
effectiveness of 19th century medicine. Analysing McKeown’s thesis, I pro-
pose adding to the institutional reasons given by Porter, historiographical
and epistemological explanations as to why the origin of bio-psycho-social
epidemiology should not be sought out in the United Kingdom (UK). The
analysis of Dubos’ thesis allows me to show that the bio-psycho-social model
that Marmot brought to the top of WHO is rooted in the United States (US).
It is fi rstly intimately linked to the emergence of a new etiological model, the
elaboration of which was grounded in a very specific interpretation of the
epistemological foundation of 19th Century social medicine. Secondly, it
found a particular destiny in the US political context, which was marked
8 In an extended Foucaultian acceptance of the term I intend to retrace the intellectual and
political statements of the actors, as well as the data they use to construct their discourses.
A detailed critical evaluation of the data, especially the way biostatistics was constructed
and analysed or judgments about the “veracity” of actor’s statements falls out of the limits
of this paper.
9 Marmot 2006, 1304.
10 Porter 2011, 165.
11 Porter 2011, p. 182.
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via free accessboth by the growing concern for chronic diseases and for racial inequalities.
That is not to say, though, that the UK context did not play a role in the de-
velopment of social epidemiology. The adoption of a transnational perspec-
tive will allow me to show how its importation and indigenization into the
UK has, in the second instance, made possible the kind of de-racialization
of bio-psycho-social social epidemiology necessary for the WHO to give
bio-psycho-social epidemiology an international aspect.
The McKeown Thesis: Setting the English Stage
Social epidemiology is today associated with some epidemiologists who, like
Marmot, have brought proof of a social determination of health to the top of
the international health institutions. Social epidemiology might appear there-
fore as a specifically Anglo-Saxon endeavour, if not purely English, for its de-
velopment came after the new figures of British social medicine of the 1950s:
John Ryle (1889–1950), Thomas McKeown (1912–1988), Jerry Morris (1910–
2009), Geoffrey Rose (1926–1993). The post-war generation that composed
what Porter calls “new public health”12 developed a strong interest in social
determinants of health as a response to their loss of faith in clinical medi-
cine.13 Dorothy Porter has demonstrated, however, how a collection of insti-
tutional and cultural factors contributed, throughout the 1960s, to the decline
of British social medicine. The interest in social determinants of diseases, re-
lying on epidemiological population analysis of the distribution of illnesses
according to social stratum, progressively gave way to an analysis of risk fac-
tors and the individual responsibility of the patient concerning their health.
This is an approach that social epidemiologists like Marmot have fiercely
contested. Focusing on the analyses of McKeown reveals exemplary reasons
why the origin of bio-psycho-social epidemiology cannot be established in
the English “new public health”.
In the 1950s, Thomas McKeown, an English physician and Professor of
Social Medicine at the University of Birmingham from 1945, published a se-
ries of articles14 that he brought together in two books, The Modern Rise of
Population15 and The Role of Medicine: Dream, Mirage, or Nemesis?16
12 Porter 2011, p. 165.
13 Porter 2011, p. 115.
14 McKeown/Brown 1955; McKeown/Record 1962.
15 McKeown 1976a.
16 McKeown 1976b.
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via free accessThese publications consider the explanations normally used for the popula-
tion increase that marked the turn of the 20th century.
Applying statistics of cause of death collected in England and Ireland
since the 1800s, McKeown demonstrates that the population increase can-
not be explained by a fall in the virulence of the infectious agent, nor by the
progressive resistance of the population to these agents. McKeown aims to
show that neither scientific medicine – chemotherapy and vaccination cam-
paigns – nor social medicine and its hygiene measures were responsible for
the significant fall in mortality rates either. For tuberculosis specifically,
McKeown demonstrates that the mortality rate began to fall in 1838, well
before the discovery of bacillus by Koch in 1882 and long before the 1940s,
which saw widespread treatment using streptomycin and vaccination by
BCG. By process of elimination, then, McKeown defends what has come to
be known as the “McKeown thesis”: the claim that the demographic and ep-
idemiological transition that began in the 18th century was not attributable
to any medical action and should instead be attributed to the rise in living
standards as a result of industrialisation. As such, the improvement of food –
McKeown considered as an epiphenomenon of the economic development
— would have made the population more resistant to a wide variety of in-
fectious diseases, in particular tuberculosis.
The McKeown Thesis engendered an array of critiques.17 Yet, it neverthe-
less established a “new orthodoxy”18 that dominated the field of public
health in the 1970s–1990s. One could ask whether the McKeown thesis has,
for epistemological reasons, played a major role in what Porter identified as
the decline in interest for social determinants of diseases in the United
Kingdom. As noted by Szreter,19 by promoting a liberal assumption that
health inequalities would “naturally” disappear along with improved living
standards accompanying the post-war economic boom – an assumption that
would later prove to be flawed20 – the McKeown Thesis led to a paradox: he
simultaneously celebrated social medicine, and, at the same time, nullified
any reason for studying how social disparities might affect health, as well as
the public health strategies that might seek to reduce them. This “lais-
sez-faire” attitude towards public health, though, contrasted sharply with the
thesis supported across the Atlantic by Dubos.
17 Condrau/Worboys 2007; Mackenbach 1996; Szreter 1988.
18 Colgrove 2002.
19 Szreter 2002.
20 For instance, Richard Wilkinson and Pickett (2009) showed that health inequalities are not
associated with absolute, but relative poverty. In other words, improving living standard
cannot reduce health inequalities on its own, whereas reducing the socioeconomic gap be-
tween the disadvantaged and the privileged can.
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via free accessThe Dubos Thesis: Setting the American Stage
These kinds of historico-epidemiological inquiries into the role played by
medicine in the eradication of infectious diseases, principally associated to-
day with McKeown’s name, were not entirely new. The subject had already
been addressed several years earlier by René Dubos. Born in France, this
agronomist by training pursued his career as a biologist in the United States.
He published several books, 21 which had some impact in the US, especially
on the radical criticism of medicine.22
Before McKeown, Dubos claimed that laboratory medicine was not re-
sponsible for the drop in mortality rate caused by tuberculosis that began to
plummet before the discovery of the infectious agents and ad hoc treatments.
Dubos, however, came to a radically different historiographic conclusion. To
him the “invisible hand”23 of economic development and the rise in living
standards do not explain the demographic explosion. According to Dubos, it
was due to the political and medical initiatives that upholders of social medi-
cine undertook in the 19th century. Villermé, Virchow and Chadwick, amongst
others, undoubtedly played a key role in putting in place better hygiene mea-
sures, increasing the cleanliness of towns and improving the quality of water
and food, etc. Yet, if these actions were indeed effective, states Dubos, it was
for ideological reasons and not based on solid scientific foundations: “the con-
quest of epidemic diseases was in large part the result of the campaign for
pure food, pure water, and pure air based not on a scientific doctrine but on
philosophical faith”.24
Social medicine, which stood in opposition to germ theory, supported a
hygienist morality with Hippocratic tendencies.25 For Dubos, there can be
no biomedical justification for the recommendations of social medicine, call-
ing for the restoration of harmony between man and the “natural” environ-
ment, a relationship hindered by industrialisation and growth in urbanisa-
tion. If Dubos grants social medicine the effectiveness that McKeown
refuses to acknowledge it, he does not discredit its scientific and political
value any less. It is precisely on this point that Dubos’s analysis advances not
only as a personal criticism of the triumphant historiography of 19th century
medicine, but also, and above all, as a systematic consideration of what the
foundations of a future medicine should be.
21 Dubos 1959 1961 1965.
22 Sedgwick 1973.
23 Szreter 2002, 722.
24 Dubos 1959, 151.
25 Dubos 1959, 145.
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via free accessCriticising further the triumphs generally attributed to scientific medi-
cine, Dubos writes:
It can be stated with great assurance that most of the persons present in the very room
where [Koch] read his epoch-making paper in 1882 had been at some time infected with the
tubercle bacilli (…). At the time, in Europe, practically all city dwellers were infected, even
though only a relatively small percentage of them developed tuberculosis or suffered in any
way from their infection. 26
If the entire population was infected with Koch’s bacillus, why did the tuber-
culosis mortality rate fall first in the better-off classes? Is it that the infectious
agent should no longer be considered the cause of disease, but rather the sus-
ceptibility of the individual determines their resistance or vulnerability to the
pathogen? Dubos expresses this displacement of the medical interrogation
process by re-appropriating the words of Bernard Shaw: “The characteristic
microbe of a disease might be a symptom instead of a cause”.27 Yet, if it is to
be believed that the figures demonstrate a drop in mortality rate caused by
tuberculosis in the better-off classes first of all, then the “susceptibility of the
host”28 directly depends upon their socio-economic status. In other words,
analysis of the social and epidemiological data has highlighted a shift con-
cerning the problem of the aetiology of disease, displacing the focus from the
infectious agent to the susceptibility of the host, and the susceptibility of the
host to the socio-economic status of the diseased person.
Dubos’ criticism drew radically different conclusions from McKeown’s.
By only attributing the fall in mortality level to the “invisible hand” of eco-
nomic development, the epidemiological transition is seen to be completely
disassociated from medical action and knowledge, whether or not these were
social or scientific. According to Dubos, in fact, “the provocative cause of
microbial disease may be a disturbance in any of the factors of his external
or internal environment – be that weather conditions, availability of food,
working habits, economic status, or emotional stress”.29 In 1965, Dubos was
more specific about the identification of environmental factors:
The microbial disease most common in our communities today arises from the activities of
microorganisms that are ubiquitous in the environment, persist in the body without causing
obvious harm under ordinary circumstances, and exert pathological effects only when the
infected person is under conditions of physiological stress. 30
26 Dubos 1959, 105.
27 Dubos 1959, 83.
28 Dubos 1959, 83.
29 Dubos 1959, 93.
30 Dubos 1965, 164.
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via free accessThe relationship between social conditions and “stress” prefigures what would
come to be the central concept of social epidemiology, that of “bio-psycho-
social stress”.
It is thus on the basis of his criticism of medicine, and the epistemological
displacement concerning the aetiology of disease, that Dubos formulated
what he imagined would be the political and scientific programme for med-
icine in the second half of the 20th century:
It is not impossible that in the future, as in the past, effective steps in the prevention of dis-
ease will be motivated by an emotional revolt against some of the inadequacies of the mod-
ern world (…) This attitude need not mean a retreat from science – far from it. The crusade
for pure air, pure water, pure food was at the best a naïve and often ineffective approach to
the problem of health of the Nineteenth Century, but it paved the way for the scientific anal-
ysis of the factor responsible for the epidemic climate of the Industrial Revolution. Simi-
larly, scientific medicine will certainly defi ne the factors in the physical environment and
the types of behaviour, which constitute threats to health in modern society. 31
To sum up Dubos’ analysis, it can be understood that the type of link that so-
cial medicine and its hygienist ideology was able to establish, between the
economic status of individuals and their vulnerability to a certain disease, re-
vealed a bio-statistical correlation at best. To Dubos, if a modern social med-
icine is to emerge, it must be supported by a testable causal physiological
model. Therefore, it is the opposition between social medicine on the one
hand, and laboratory medicine on the other, which must be reconsidered with
the aim of clarification. Laboratory medicine, which until then had focused
all its attention on the isolated external cause – the mono-causal infectious
agent – should look towards incorporating the susceptibility of the host into
its research including psychosocial variables in its protocol. Doing so, it
would be able to replace social medicine’s ideological justification with ex-
perimentally justified explanations. This is the analysis and related research
program elaborated by Dubos that the first generation of bio-psycho-social
epidemiologists, such as John Cassel, would go on to carry out based on what
Dubos identifies as an “emotional revolt” against racial health inequalities.
31 Dubos 1959, 219.
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via free accessSocial Epidemiology: Racial inequalities before the Bio-Psycho-Social
Model
According to the American Constitution, ratified in 1787, the “people of the
United States” are the sovereign political authority of the nation. Accord-
ingly, Article I, Section 2 states that:
Representatives and direct taxes shall be apportioned among the several states which may
be included within this union, according to their respective numbers, which shall be deter-
mined by adding to the whole number of free persons, including those bound to service for
a term of years, and excluding Indians not taxed, three fi fths of all other Persons. The ac-
tual Enumeration shall be made within three years after the fi rst meeting of the Congress
of the United States, and within every subsequent term of ten years, in such manner as they
shall by law direct.
The representation of the sovereign people thus requires a federal census to
determine, in proportion to the population of each state, the amount of fed-
eral taxes they will have to pay, as well as the number of seats they will have
in the House of Representatives. To this end, the U.S. Census Bureau was
formed every decade until 1902, when it was perpetuated.
In this context, the status of individuals resulting from the slave trade be-
comes a central political issue. The representatives of the southern states, in
favour of slavery, had the largest population of slaves. They therefore had a
strong interest in defending their census in order to obtain more seats in the
House of Representatives. The northern states, in favour of the liberation of
slaves, rejected the proposal on the pretext that slaves could not be both
property and representative citizens. A compromise was reached: each state
would count the free individuals, to which would be added three-fi fths of the
“other persons”. On this basis, the fi rst census, conducted in 1790, counted
white men and women and slaves.
The office’s mission was originally limited to the census of inhabitants, it
meant by no means to collect vital statistics. It was around the 1840s, based
on the methods implemented in England and Wales under Chadwick’s lead-
ership, that the fi rst registers of births, deaths and causes of death were cre-
ated. It was not until the end of the civil war that the American Public
Health Association was founded in 1872 and then, in 1879, the National
Board of Health, which aimed to generalize the collection of vital statistics
at the national level.
In 1880, John Shaw Billings, a former medical statistician in the Potomac
army, became president of the National Board of Health’s Committee on
National Statistics and was responsible for organizing the decennial census.
In 1890, the fi rst “modern” census was issued, incorporating vital statistics.
When in 1946 the responsibility for collecting biostatistics was transferred
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via free accessfrom the Census Office to the National Office of Vital Statistics of the U.S.
Public Health Service, racial categories could have disappeared. They were,
however, renewed as they stood. In the meantime, the availability of epide-
miological data, has allowed US public health institutions to show the exis-
tence of a racial gap.
To Krieger, the term “social epidemiology” first appeared in a paper by
Alfred Yankauer, 32 a Harvard graduate and of Professor of Family and
Community Health at the University of Massachusetts from 1973 to 1990.
At the end of three years training spent as a Health Officer for the New
York City Department of Health, Yankauer published a study based on the
1940 census figures. The paper, entitled “The Relationship of Foetal and In-
fant Mortality to Residential Segregation: An Inquiry into Social Epidemi-
ology”, 33 demonstrates that: “in New York City neighbourhoods both white
and Negro foetal and infant mortality rates increase as the proportion of Ne-
groes in the neighbourhood increases”. 34 Yankauer explains that in the over-
populated ghettos rent prices are proportionately higher, hygiene conditions
poorer and access to high quality and varied foods is more limited. Members
of the black community are faced with materially degraded living conditions
and oversubscribed medical institutions. Weaker fi nancial resources for
food and healthcare further exacerbate this. Yankauer’s study closes with a
plea for taking large-scale action for desegregation by breaking down the
barriers causing residential division.
Yankauer’s integration of social epidemiology into social medicine, is not
only apparent in the reference to Virchow that concludes his paper: “Medi-
cine is a social science and politics nothing but medicine on a grand scale.”
It is also apparent on the epistemological front. To him, social epidemiology
remained an analysis of the socioeconomic material conditions of health. It
limited itself to the correlation between the state of health and accessibility
to certain necessities, such as quality of food or access to adequate health-
care. Moreover, the term “social epidemiology” appeared as limited to re-
vealing sociological correlations. It did not, therefore, offer analysis of the
pathophysiological mechanisms, i.e. the physiological vulnerability or sus-
ceptibility to diseases, likely to explain the causal link between social status
and the state of health of an individual. By incorporating a racial factor,
Yankauer did introduce a new social determinant. He did not, however, han-
dle racism in terms of being a social construct concerning racial/social rela-
tions. He reduced it, rather, to simply considering geographical segregation.
32 Yankauer 1950.
33 Yankauer 1950.
34 Yankauer 1950, 646.
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via free accessThis is the very reason why Yankauer claims that as the “proportion of Ne-
groes” rises, foetal mortality rises both for white and black people. Racial
relations are thus reduced to being structural socioeconomic components
concerning material living conditions or level of access to certain goods or
services. If one can suppose that those determinants truly induce a “physi-
ological stress”, their influence is indistinguishable from racial/social status.
In other words, Black people living in a white neighbourhood would have
the same foetal mortality as their white peers. Finally, this social epidemi-
ology essentially remains an epidemiology of social resources and physio-
logical “lacks” of primary physiological needs, and healthy environments. It
always presupposes – something McKeown would not have disapproved of –
that a general improvement in living standards (better access to decent food,
to medical care etc.) leads systematically to an improvement in health.
If so, the economic boom in the US should have been accompanied by an
improvement in the living standards of African-Americans. If the increase
in living standards did improve health in the African-American commu-
nity35, the racial gap between blacks and whites remained and was trans-
ferred to include chronic diseases that are associated with the development
of industrialized societies. As we will shall see, modern social epidemiology
emerged exactly when the explanations mobilized in order to account for ra-
cial health inequalities in the US, especially chronic disease, switched focus
from the external pathogenic conditions or agents (the presence of a noxious
agent or the lack of access to primary needs), to the social conditions deter-
mining what Dubos called the susceptibility of the host.
Chronic Disease within an Ethnocentric Pathophysiology
George Weisz36 documented how US public health institutions, more quickly
than other nations, gradually transferred their focus from communicable dis-
eases – that were not considered as the major cause of death anymore – to
chronic diseases. The reorganisation of the health services at the beginning
of the 20th century37 then by the “Welfare” politics following the “New Deal”
initiated by Roosevelt at the brink of the 1929 crisis, fed a deep concern for
what was identified as an “unseen plague”.38 Armstrong39 has shown how in
35 Williams 2001.
36 Weisz 2014.
37 Weisz 2014, 30.
38 Boas, 1940.
39 Armstrong, 2014.
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via free accessthe first half of the 20th century, it has widely been agreed that a rise in life
expectancy causally explained the rise in the prevalence of degenerative dis-
eases such as hypertension. In 1934, Charles Stone confi rmed, “Arterioscle-
rosis, as we know it, is bound by the laws that govern the average age of a spe-
cies. It is ultimately inevitable, therefore, and not subject to change”.40 Arte-
rial hypertension was then generally seen to be “essential”, i.e. the result of
the natural degeneration of vascular tissue occurring in an aging population.
This idea was apparently corroborated by epidemiological statistics demon-
strating that hypertension affects the entire population and its prevalence
gradually increases with age. If the disease is essential, then the medical pro-
fession can only delay the effects of an inevitable process. It was necessary to
wait until the 1950s, when the first results of the Framingham Heart Study
were issued and the notion of (individual) risk factor emerged for behavioural
aspects (alcohol consumption, lifestyle etc.) and predisposing conditions (hy-
pertension, obesity, cholesterol etc.) to challenge the theory of the “essenti-
ality” of hypertension. Yet, another and less documented field of research,
focusing on solving what appeared to be an enigma, the high prevalence of
hypertension in the African-American community, also contributed to these
transformations.
In the 1930s, census figures had already revealed that black people suffer
more pathologies and have a higher death rate than white people. The eval-
uation of the impact of chronic disease on economic life also revealed a ra-
cial disparity. Black workers had a higher level of invalidity than white work-
ers41 and it is also notable that in a workforce employed by the same
company, black workers tended to have a higher blood pressure than white
workers.42 More importantly, the figures from the 1930s to the 1960s census
demonstrate a strong and ever-increasing prevalence of a specific disease in
the African-American community – arterial hypertension – the causes of
which remained hypothetical.
In 1957, Lennard and Glock43 listed four hypotheses along with their re-
spective limitations. (1) The hypothesis of “physical exertion” incorporates
the theory of the “economic gap”: African-Americans work in the lowest
paid professions and those that, as a result, require the greatest physical ef-
fort. There is no data, however, to suggest a link between physical effort and
a rise in blood pressure. On the contrary, physical activity has been seen to
reduce the risk of coronary disease. (2) Abram Kardiner and Lionel Ove-
40 Stone, 1934.
41 Britten 1934.
42 Adams 1932.
43 Lennard/Glock 1947.
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via free accesssey44 suggested an alternative explanation: hypertension could be linked to
“psychological confl icts” that are the result of suppressed feelings of aggres-
sion and emotional stress induced by the psychological pressure placed by
whites on African-Americans. Lennard and Glock note, however, that this
psychoanalytically inspired theory could not be validated as it was only
based on interviews that took place with 25 individuals. (3) The “associated
disorders” hypothesis views hypertension as a disease associated with syph-
ilis or pyelonephritis. For the authors, the studies on the subject seem,
though, to lead to contradictory results. (4) Finally, the theory of a genetic
trait that predisposes Black people to hypertension always fi nds its defend-
ers. The authors note, however, that the figures here are lacking. To validate
this theory, it would be necessary to demonstrate that “a racial disposition
to hypertension would be manifested in a higher occurrence of hypertension
among Negroes than among whites wherever they may be located”.45
The problem of the prevalence of arterial hypertension in general, and in
the African-American community in particular, might thus require compar-
ative physiological study. By questioning the universality of the general pat-
tern of arterial tension recorded in the western world, epidemiologists oper-
ated a major epistemological reconfiguration. By introducing the concept of
“cross-cultural” epidemiology of hypertension,46 they acknowledged that
biomedicine raised the physiological parameters of the white man to the
rank of being normal, natural and thus, universal. As we shall see, in assum-
ing that physiology might have had ethnocentric presuppositions – a meth-
odological bias believed to be limited to the social sciences – cross cultural
epidemiology fi nally opened the way for a study of the physiological param-
eters, incorporating hitherto unseen variables, be they racial, cultural or so-
cio-economic.
Towards a Socio-Cultural Epidemiology of Hypertension
Validation of the essentialist thesis required that the cultural variability of
arterial hypertension be tested. The cross-cultural epidemiology of hyper-
tension was an important step towards displacing the focus from cultural to
social determinants of hypertension. I will here re-examine this change of fo-
cus to show how it progressively oriented epidemiologists towards identifying
44 Kardiner/Ovesey 1951.
45 Lennard/Glock 1957, 191.
46 Lennard/Glock 1957, 192.
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via free accesssocial stress, rather than any ineluctable biological determinism, as a main
aetiological factor for hypertension.
In a review paper Jack Geiger and Norman A. Scotch47 count over one
hundred studies aimed at measuring the “socio-cultural” variability of arte-
rial tension. The oldest dates back to 1916.48 Out of these hundred or so
studies, only nineteen demonstrate homogenous samples allowing for the
comparison of twenty-two different societies on the basis of age and sex. The
authors reveal a certain variability concerning the average blood category
for people aged from 46 to 65 years old. The lowest result for both sexes
(105/68) is found amongst the Kuna Indians from the north of Colombia.
The highest measurement of blood pressure was recorded amongst the in-
habitants of the United States Virgin Islands.49 The results recorded in this
group of Caribbean Islands under American administration since 1917, en-
abled comparison of the vital statistics of black and white inhabitants of the
archipelago, and could then be compared with Americans living on the
mainland. In the US, the average blood pressure is between 142/85 for men
and 144/85 for women. In the white community of the Virgin Islands it is
146/86 for men and 148/86 for women. In the black community, this rises to
156/93 for men and 169/98 for women. For Geiger and Scotch, the fact that
whites on the Virgin islands have a higher blood pressure than Americans
on the mainland leads them to believe that the difference is mainly the re-
sult of socio-economic factors affecting all “races” and, in particular, the
Blacks, who are the least materially privileged: “the inhabitants of the Vir-
gin Islands are generally poor; they suffer from vitamin deficiencies; and
both negroes and whites have higher blood pressure than persons in the
United States”. 50 For others, though, such as Alfred Moser, this study, as
well as others that are similar carried out in the Belgian Congo, Ruanda
Urundi, North Rhodesia, Liberia and South Africa, seems to corroborate
the theory that “elevated blood pressure does occur even in some primitive
tribes”. 51
It is pertinent here to establish the author’s understanding of “primitive
tribe”. Moser is fully aware of the fact that the studies carried out up to then
were subject to methodological misgivings hindering a true physiological
47 Geiger/Scotch 1963.
48 Concepcion/Bulatao 1916.
49 Saunders/Bancroft 1942.
50 Saunders/Bancroft 1942, p. 422.
51 Moser 1960, 989.
48 Gesnerus 77 (2020)
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via free accesscomparison likely to determine if hypertension found amongst Afri-
can-Americans is genetically caused or not:
Unfortunately, until now direct comparisons of data on the prevalence of hypertension
among Negroes from Africa and the United States have not been possible since adequate
blood pressure surveys have not been carried out on the west coast of Africa (Ghana, Libe-
ria, and French Equatorial Africa), the points of origin for Negroes brought to the New
World. Most of the data reported to date has been from South Africa and east Africa, ar-
eas where the population may differ considerably from the American Negro. 52
Moser notably refers to a study carried out in South Africa53 involving post
mortem analysis of the cardiovascular systems of 194 white South Africans
of European origin and 346 of the Bantu peoples, a linguistic community,
that although migrating east as well as south in Africa originally came from
west Africa. The authors, however, show that in their cohort, “the majority
of the adult Bantu subjects spent their childhood in rural areas and moved to
urban areas after the age of about 16 years”.54 In a similar way, Moser’s study
was also meant to involve “primitive people”, and in fact involved “the entire
populations of two small villages separated by approximately 50 miles in Li-
beria, Africa, and of young, healthy male tappers at the Firestone Plantation
in Liberia”. 55 In both cases, just like in the Virgin Islands study, the popula-
tions termed “primitive” come in fact from towns, rural village settlings or
even plantations. The choice of populations is therefore full of assumptions
according to which there is a predisposition towards hypertension indepen-
dent from social environments (rural, town, plantations …).
Scotch56 carried out his own study of “socio-cultural” factors of hyperten-
sion in order to avoid these pitfalls. During a two-year long research trip in
South Africa he studied the blood pressure levels of a group of Zulus living
in a reserve that, in spite of living in a certain amount of poverty, maintained
a traditional way of life relatively unaffected by Apartheid. Their blood
pressure was compared with that of the Zulus that migrated, for economic
reasons, to Durban where “police harassment and arrest, a daily fact of life,
must be seen as stressful in the extreme”. 57 The blood pressure of the two
groups of Zulus was eventually compared with that of the white community
and that of the African-Americans of Comstock, Georgia, in the south of
the United States. These measurements allowed Scotch to reveal a so-
cio-cultural gradient: “the rural Zulu have the lowest mean blood pressure,
52 Moser 1960, 989.
53 Meyer et al. 1964.
54 Meyer et al. 1964, 415.
55 Moser, p. 993.
56 Scotch 1963.
57 Scotch 1963, 1205.
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via free accessthe white Georgians are somewhat higher, the urban Zulu are still higher,
and the Georgia Negroes are highest of all”. 58 Since the rural Zulus show a
lower blood pressure than the white population in the United States, the
theory of an intrinsic deficiency of the “black race” seems to lose all valid-
ity. It is further weakened by the fact that the study demonstrates a correla-
tion between duration of residence in the city and rise in blood-pressure:
“the longer the residence, the more the hypertension”. 59
Yet, if we return to the summary article of Geiger and Scotch, which de-
tails nineteen studies comparing twenty-two different societies, it is note-
worthy that, although black men and women from the Virgin Islands have
the highest blood pressure, the lowest was recorded in the Kuna Indian com-
munity. Not only is it low, but it is also equal for both sexes and shows no
variation according to age. Recognisable here, is the characteristic pattern
of blood pressure such as it has been measured in truly “primitive” popula-
tions, i.e. populations where the social organisation has not been affected by
sedentariness, agriculture and industrialisation. In 1967, collaborations be-
tween cardiologists, epidemiologists and anthropologists allowed for the
study of completely undisturbed hunter-gatherer communities in West Af-
rica.60 The results, ratified many times since,61 attested to the fact that the
pattern of blood pressure in the Kuna Indians, low for both sexes and not
increasing with age, is unique to the hunter-gatherer communities. These re-
sults helped to establish a theory of social variability of hypertension, given
that it is primarily the type of socio-economic organisation, more than cul-
ture, which proves to be decisive. The causal connection between stress and
social structure, however, still required clarification.
John Cassel: A Bio-Psycho-Social Epidemiology
During the 1960s, the hypothesis that bio-psycho-social stress causes arterial
hypertension in the African-American population was still based on epide-
miological correlations. As we shall see, the combination of Dubos’ pro-
gramme of research, on the one hand, and the epidemiology of hypertension
58 Scotch 1963, 1207.
59 Scotch 1963, 1208.
60 Epstein/Eckoff 1967.
61 This was only briefly contested by the hotly debated bio-historical hypothesis of Wilson/
Grim 1991, which stated that slaves possessing a sensitivity to salt, therefore retaining more
sodium and water, would have had a selective advantage allowing them to withstand the
transport conditions to America as well as the conditions of life on a plantation. For a cri-
tique see Curtin 1997.
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via free accesson the other, allowed John Cassel to provide a causal relation and redefine
the object of social epidemiology as the study of the bio-psycho-social deter-
minants of disease. Once again, arterial hypertension in the African-Amer-
ican community played a paradigmatic role.
In 1970, Sole Levine and Scotch published a collection of works under the
title Social Stress. For the authors, this publication developed because, until
then, no “systematic discussion of the conceptual and methodological issues
of the sources and the consequences of social stress”62 existed. The preva-
lence of arterial hypertension in the African-American community appears
as a paradigmatic example:
We can agree that Negroes suffer from more stress experiences and also have a higher prev-
alence of hypertension. Unfortunately, it is at this point that epidemiologists – at least until
recently – have failed to pursue the question and to test the relationship of stress experi-
ences to the development of hypertension.63
Why have things recently changed? In fact, the work of John Cassel, who
contributed to the publication,64 made significant headway in the field. For
Cassel, the mass of epidemiological cross-cultural data cannot alone provide
the answer to the question of the non-universality of hypertension, but it at
least constitutes a guiding light of evidence:
Despite the weakness of each study taken individually a rather extraordinary concordance
of results is obtained when reviewing all the studies simultaneously. Thus studies on the
level of blood pressure conducted over the last 30 years in many countries across the world
(…) have universally shown populations living in small cohesive societies “insulated” from
the changes that are occurring in the Western industrializing countries, with low blood
pressure that do not differ in the young and the aged.65
By explicitly transposing Dubos’ conceptions of socially determined “suscep-
tibility of the host”, from infectious to chronic disease, Cassel deduces:
From the data summarized thus far, it would appear not unreasonable to expect that the
more precise identification of some of the social processes hinted at could yield important
new information on some of the sources of physiological stress that Dubos maintains “con-
vert latent infection into overt symptoms and pathology.66
The short yet prolific career of Cassel contributed towards bringing the aeti-
ological displacement highlighted by Dubos into the field of social epidemi-
ology in general, in order to apply it more specifically to its prototypical ob-
ject. Biographical reasons may explain Cassel’s interest in the prevalence of
high blood pressure in the African-American community. Cassel came from
62 Levine/Scotch 2013[1970], 10.
63 Levine/Scotch 2013[1970], 5.
64 Cassel 2013[1970].
65 Cassel 2013[1970], 196.
66 Cassel 2013[1970], 200.
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via free accessSouth Africa where he developed clinics for Zulu groups that lived in the
margins of South African society. When Apartheid was in full force in 1948,
all racial mixing, including medical practice, became illegal and was punish-
able by death. Cassel and his wife, a nurse, were exiled from the country in
1953. They landed in England before settling definitively in the US, where he
became the Director of the Department of Epidemiology School of Public
Health at the University of North Carolina in 1958. Despite the lack of infor-
mation available concerning Cassel’s life, his political commitments can be
indirectly presumed. Cassel belongs to a generation of South African doc-
tors, nurses, and epidemiologists, forced into exile and established in the US
because of their will to develop socio-medical institutions devoted to racial
minorities. Emily and Sidney Kark were also forced into exile in 1958 and
Zena Stein and Mervin Susser were expelled in 1955. One can imagine that
Cassel shared the views of the latter who was overtly militant against the
Apartheid and for social justice, not hesitating to put the situation of African
minorities in South Africa and African-Americans into perspective in the
US.67 Consequently, Cassel had many reasons to be “emotionally revolted”
by racial health inequities (to use Dubos’ words) and sensitive to the civil
rights movement dominating the US throughout the 1960s–1970s. Endeav-
ouring to provide experimental and neurophysiological justification for the
epidemiological correlations, he set about literally carrying out the political
and scientific programme envisaged by Dubos.
A year prior to his contribution to Levine and Scotch’s book in the Amer-
ican Journal of Epidemiology, Cassel published an article with the physiol-
ogist James Henry.68 In it, they detail the general spectrum of data consid-
ered to be potential causes of high blood pressure. Cross-cultural
epidemiology, however, seemed to indicate that the risk factors generally
suggested by epidemiologists – diet, tobacco, salt consumption, obesity or
even inheritance – were only aggravating factors rather than the direct and
external causes of hypertension. The two authors refer to a study led by
Henry, which involved isolating young mice from their birth before reintro-
ducing them into the “social” group at maturity. Henry compared the phys-
iological effects of diet (intake of caffeine, salt etc.) to those of the disorgan-
isation of the “social hierarchy”. If diet seemed to have little effect, chronic
“social stress”, experimentally induced, strongly correlated with the appear-
ance of peptic ulcers and high blood pressure.
67 See for instance Susser 1983.
68 Henry/Cassel 1969.
52 Gesnerus 77 (2020)
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via free accessFor Cassel, Selye’s General Adaptation Syndrome69 combined with Du-
bos’s conception of the susceptibility of the host, was the kind of integrative
explanation that could causally explain how bio-psycho-social stress causes
disease in general and hypertension in particular. To Selye, chronic stress
engendered by the effort necessary to adapt, leads, via activation of the hy-
pothalamus and the pituitary gland, to a reaction of alarm, followed by re-
sistance, then a state of general exhaustion at which point multiple diseases
appear.70 Cassel does not hesitate to make the connection between the “so-
cial deprivation” experienced by mice and the mortality rate linked to car-
dio-vascular disease:
The alarm response induces modifications of the steady state condition, which activate
adaptive mechanisms. There is evidence that by acting repeatedly over the years, this de-
fence reaction will lead to a chronic elevation of systolic arterial pressure in the majority of
the members of a disturbed social group.71
Cassel found, in Henry’s experiments with mice, the operationalization of
Dubos experimental project, which aimed to bring “social” variables into the
laboratory. Yet, Cassel also extended Dubos’ experimental appeal outside
the laboratory. It was through his efforts to objectivise the causal links be-
tween stress and social relationships that the case concerning the prevalence
of high blood pressure in the African-American community reappeared as a
paradigmatic case study. Cassel led a research project with Neser72 studying
the mortality rate as a result of cardio-vascular attack in one hundred coun-
ties of North Carolina classed according to the Smith Index. The index gives
a score of “social disorganisation” considering family instability, illegitimate
birth rate, rate of imprisonment and divorce rate. The study revealed, in the
African-American community, and not in the white community, a correla-
tion between mortality rate and the level of social disorganisation. Addition-
ally, this gradient proved to be independent of absolute poverty of individu-
als and of physical environmental conditions. Coming back to these findings
in 1976, Cassel concluded:
In animal experiments, changes in the social milieu have their most marked and dramatic
effects on the health and endocrine status of subordinate animals, with dominant ones
showing the least effects. Perhaps these fi ndings reflect the subservient role the Blacks (un-
til perhaps recently) have been forced to occupy in our society. The second speculation is
the possibility that in the face of social disorganization Whites have more resources, includ-
ing sources of social support to help buffer their physiologic processes from these effects.73
69 Selye 1952.
70 For a detailed study on the history of stress and its links with social epidemiology see
Arminjon 2016.
71 Henry/Cassel 1969, 1895.
72 Neser/Tyroler/Cassel 1971.
73 Cassel 1976, 116.
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via free accessDue to his premature death in 1976, Cassel could not continue his research.
His work did, nevertheless, go on to profoundly affect future developments
in social epidemiology.
For instance, Nancy Krieger, a figurehead in American social epidemiol-
ogy, acknowledges, in a theoretical paper, that social epidemiology benefit-
ted substantially from Cassel’s findings (Dubos only earns a footnote).74 But
she also points out that the bio-psycho-social framework pays too much at-
tention to physiological resources and not enough to the social, political and
economic policies that generate psychosocial inferiorities. Paradoxically, de-
spite her critics, her empirical work is firmly rooted in the US social epidemi-
ological tradition from which she employs the epistemic object and bio-psy-
cho-social model. In 1996, Nancy Krieger, and Stephen Sidney, published
their research, the significance of which is summarised in the following way:
“our results indicate that racial discrimination shapes patterns of blood pres-
sure among the US Black population and Black-White differences in blood
pressure”.75 They were able to measure that African-Americans claiming
never to have experienced racial discrimination had higher blood pressure
than those who recognised that they had been the object of discrimination
and were in the habit of fighting against it. They thus brought back into fash-
ion the theory supported thirty years earlier by Abram Kardiner and Lionel
Ovesey76. Racism, redefined as stress induced by social stigma, is one of the
psychosocial causes of high blood pressure, especially when internalised.
Like Cassel, they demonstrated that the fact of being black in the USA im-
plies assuming a social “role” which determines state of health even more
than absolute poverty. This social role not only determines the type of rela-
tionships that individuals share with their community and the rest of society,
but, moreover, their inner life, both psychologically and biologically. Indeed,
individuals inclined to share and condemn their experiences of discrimina-
tion create around themselves the community and social support required to
buffer the detrimental physiological effect of social stigmatization.
Bio-psycho-social Epidemiology: From the Local to the Global
If the work of Krieger, amongst others,77 testifies to the fact that social epi-
demiology is not historically dissociable from the racial issues specific to the
74 Krieger 2001, 670.
75 Krieger/Sidney 1996.
76 Kardiner/Ovesey 1951.
77 Williams 2001.
54 Gesnerus 77 (2020)
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via free accessUS’s public health system, we are bound to go on to consider the process of
transnational circulation that de-racialized the discipline and made it an in-
ternational health issue.
After an undergraduate degree in medicine Marmot undertook a Ph.D.
at the Berkeley School of Public Health, under the direction of Syme, a so-
ciologist given the title of professor of epidemiology in 1968. Syme78 sug-
gested he study the case of Japanese people living in California who found
themselves five times more likely to contract coronary heart disease than
people living in Japan. Marmot demonstrated that the Japanese living in
California, who had maintained a traditional style of life, had no more of a
coronary risk than the Japanese living in Japan.79 Syme’s influence on Mar-
mot was two-fold.
Firstly, Syme remains attached to the bio-psycho-social model. He admits
the debt his work owes to Cassel.80 For instance, in an article seeking to
open the way for future research in social epidemiology, Syme and Berkman
state: “The proposal offered here is that those in the lower classes consis-
tently have higher rates of disease in part due to compromised disease de-
fences and increased general susceptibility”.81 The notion of “general suscep-
tibility” here invokes Dubos by way of Cassel. Secondly, this passage also
demonstrates that if Syme aligns himself with American public health is-
sues, he also distances himself from them. By introducing the notion of “so-
cial class”, he recognises that American social epidemiology is intimately
linked to the health inequalities suffered by racial minorities and that these
local public health issues should not hide the fact that general susceptibility
to diseases concerns all the social classes. Syme, in fact, recalls that if Black
people have a higher rate of hypertension than white people, a “social class
gradient”82 can also be measured within the African-American community,
as well as within the white community. For Syme, these facts “suggest that
something about lower social class position may be involved over and above
any racial influences”.83 It is both the bio-psycho-social model and the con-
cept of the social gradient, expanded to incorporate all social classes and not
simply the African-American community, that Marmot went on to import
and implement in the United Kingdom.
With his Ph.D. completed in 1976 Marmot joined the London School of
Hygiene and Tropical Medicine. There he encountered Geoffrey Rose, one
78 Syme 2005.
79 Marmot/Syme 1976.
80 Syme 2005.
81 Syme/Berkman 1976, 6.
82 Syme et al. 1974, 619.
83 Syme et al. 1974, 620.
Gesnerus 77 (2020) 55
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